AIM: To investigate the protective effect of glutamine (Gln) on intestinal injury and the bacterial community in rats exposed to hypobaric hypoxia environment.
AIM To investigate the modulatory effect of recombinantexpressed vasoactive intestinal peptide(VIP) analogue(rVIPa) on trinitrobenzene sulfonic acid(TNBS)-induced colitis in rats. METHODS Forty-eight rats were randomi...AIM To investigate the modulatory effect of recombinantexpressed vasoactive intestinal peptide(VIP) analogue(rVIPa) on trinitrobenzene sulfonic acid(TNBS)-induced colitis in rats. METHODS Forty-eight rats were randomized into six groups: normal control group(Control), model control group(TNBS), ethanol treatment group(ETOH), and VIP treatment groups with different dosage(rVIPa_(1nmol), rVIPa_(2nmol), rVIPa_(4nmol)). Diarrhea and bloody stool were observed. Colonic damage was evaluated histologically. The levels of tumor necrosis factor-α( TNF-α), interleukin-10(Il-10), myeloperoxidase(MPO) and endotoxin in colonic tissue and serum were determined by enzyme-linked immunosorbent assay(ElISA). The expression of occludin, ZO-1, Toll-like receptor 4(TlR4),and nuclear factor-kappa B p65(NF-κBp65), IκBα, and p-IκBα were detected by Western blot. RESULTS Administration with 2 nmol rVIPa prevented TNBSinduced necrosis, hyperemia, swelling, inflammation, etc., pathologic changes observed in the inner surface of colon in experimental rats. Moreover, rVIPa significantly decreased colonic TNF-α level(P < 0.001), MPO activity(P < 0.001) and serum endotoxin level(P < 0.01), and remarkably increased colonic Il-10 content(P < 0.001) in rats with TNBS-induced colitis. Furthermore, compared to the TNBS-induced colitis group, 2 nmol rVIPa treatment up-regulated the levels of occludin(P < 0.05) and ZO-1(P < 0.05), NF-κB p65(P < 0.01) and IκBα(P < 0.001), and down-regulated the levels of TlR4. CONCLUSION rVIPa ameliorates TNBS-induced colonic injury and inflammation and effectively protected the intestinal mucosal barrier function in rats. The mechanism may be related to TlR4/NF-κB-mediated signaling pathway. rVIPa could be used as a new alternative therapy for intestinal inflammatory disorders.展开更多
基金Supported by National Natural Science Foundation of China,No.31001012 and No.31101304Programs for Agricultural Science and Technology Development of Shaanxi Province,China,No.2013K02-16Northwestern Polytechnical University Foundation Science Research Fund,No.JC201278
文摘AIM: To investigate the protective effect of glutamine (Gln) on intestinal injury and the bacterial community in rats exposed to hypobaric hypoxia environment.
基金Supported by the National Natural Science Foundation of China,No.31672435the Graduate Starting Seed Fund of Northwestern Polytechnical University,No.Z2017236the National College Students Innovation,Experiment Program,No.201610699266
文摘AIM To investigate the modulatory effect of recombinantexpressed vasoactive intestinal peptide(VIP) analogue(rVIPa) on trinitrobenzene sulfonic acid(TNBS)-induced colitis in rats. METHODS Forty-eight rats were randomized into six groups: normal control group(Control), model control group(TNBS), ethanol treatment group(ETOH), and VIP treatment groups with different dosage(rVIPa_(1nmol), rVIPa_(2nmol), rVIPa_(4nmol)). Diarrhea and bloody stool were observed. Colonic damage was evaluated histologically. The levels of tumor necrosis factor-α( TNF-α), interleukin-10(Il-10), myeloperoxidase(MPO) and endotoxin in colonic tissue and serum were determined by enzyme-linked immunosorbent assay(ElISA). The expression of occludin, ZO-1, Toll-like receptor 4(TlR4),and nuclear factor-kappa B p65(NF-κBp65), IκBα, and p-IκBα were detected by Western blot. RESULTS Administration with 2 nmol rVIPa prevented TNBSinduced necrosis, hyperemia, swelling, inflammation, etc., pathologic changes observed in the inner surface of colon in experimental rats. Moreover, rVIPa significantly decreased colonic TNF-α level(P < 0.001), MPO activity(P < 0.001) and serum endotoxin level(P < 0.01), and remarkably increased colonic Il-10 content(P < 0.001) in rats with TNBS-induced colitis. Furthermore, compared to the TNBS-induced colitis group, 2 nmol rVIPa treatment up-regulated the levels of occludin(P < 0.05) and ZO-1(P < 0.05), NF-κB p65(P < 0.01) and IκBα(P < 0.001), and down-regulated the levels of TlR4. CONCLUSION rVIPa ameliorates TNBS-induced colonic injury and inflammation and effectively protected the intestinal mucosal barrier function in rats. The mechanism may be related to TlR4/NF-κB-mediated signaling pathway. rVIPa could be used as a new alternative therapy for intestinal inflammatory disorders.
